* 12 Flashcards

1
Q

chromosomes

A
  • building material: chromatin – complex of DNA + proteins
  • each consists of one very long, LINEAR DNA molecule associated w/ many proteins
  • when not dividing, each chromosome is in the form of a long, thin chromatin fiber; condenses (coils and folds) only after DNA replication
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2
Q

sister chromatids

A
  • each chromatid contains an identical DNA molecule
  • initially attached all along their lengths by protein complexes called COHESINS; this attachment is known as SISTER CHROMATID COHESION
  • each sister chromatid has a CENTROMERE, a region containing specific DNA sequences where the chromatid is attached most closely to its sister chromatid (this attachment is mediated by proteins bound to the centromeric DNA sequences)
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3
Q

kinetochore

A
  • structure of proteins associated w/ specific sections of chormosomal DNA at each centromere
  • spindle microtubules attach during prometaphase
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4
Q

polar microtubules

A
  • microtubules that don’t attach to kinetochores
  • elongate
  • by metaphase they overlap and interact w/ other nonkinetochore microtubues form the opposite pole
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5
Q

cell elongation

A
  • nonkinetochore microtubules do it during anaphase
  • nonkinetochore microtubules from opposite poles overlap e/o extensively during metaphase; during anaphase, the region of overlap is reduced as motor proteins attached to the microtubues walk them away from one another, using energy from ATP
  • as the microtubues push apart from e/o, their spindle poles are pushed apart, elongating the cell
  • at the same time, the microtubules lengthen somewhat by the addition of tubulin subunits to their overlapping ends, so the microtubules continue to overlap
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6
Q

chromosomal poleward movement

A
  • “Pacman” mechanism: motor proteins on the kinetochores “walk” the chromosomes along the microtubules, which depolymerize at their kinetochore ends after the motor proteins have passed
  • chromosomes are “reeled in” by motor proteins at the spindle poles; microtubues depolymerize after they pass by these motor proteins
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7
Q

cytokinesis

A

begins during anaphase/telphase

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8
Q

cell cycle time

A
  • interphase: 90 percent
  • M phase: <1hr
  • S phase: 10-12 h
  • G1: 5-6 h (most variable in length in diff cell types)
  • G2:4-6 h
  • each cell: 1 division in 24 hours
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9
Q

cleavage furrow

A
  • shallow groove in cell surface near the old metaphase plate
  • on the cytoplasmic side is a contractile ring of actin microfilaments associated w/ myosin molecules
  • the two proteins interact, causing the ring to contract
  • the contraction of the microfilament is like the pulling of a drawstring
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10
Q

bacterial proteins

A
  • one resembling actin functions in chromosome movement

- one related to tubulin helps pinch plasma membrane inward

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11
Q

binary fission

A
  • cell grows to 2x its size then divides to form 2 cells
  • initiated when the DNA begins to replicate at a specific place on the chromosome called the ORIGIN OF REPLICATION
  • soon after, one origin copy moves toward the other end of the cell
  • replication finishes, plasma membrane grows inward, new cell wall deposited, 2 daughter cells result
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12
Q

cell division: dinoflagellates

A
  • chromosomes attach to nuclear envelope, which remains intact during cell division
  • microtubules pass thru nucleus inside cytoplasmic tunnels, reinforcing the spatial orientation of the nucleus, which then divides in a process reminiscent of bacterial binary fission
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13
Q

cell division: diatoms and some yeasts

A
  • nuclear envelope remains intact
  • microtubues form spindle within nucleus
  • microtubues separate chromosomes; nucleus splits into 2 daughter nuclei
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14
Q

G0 phase

A
  • G1 checkpt is most impt
  • if go-ahead signal isn’t received, cell will exit cycle, switching into nondividing state called G0
  • most cells of human body are in G0 phase
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15
Q

anaphase

A
  • commences suddenly when the cohesins holding together the sister chromatids of each chromosome are cleaved by an enzyme called SEPARASE
  • once the chromatids become separate, full-fledged chromosomes, they move toward opposite ends of the cell
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16
Q

cell cycle regulatory molecules

A
  • protein kinases: give go-ahead signals at G1 and G2
  • many of these kinases are actually present at a constant concentration in the growing cell, but much of the time they’re in inactive form; to be active, they must be attached to a CYCLIN, a protein that gets its name from its cyclically fluctuating concentration in the cell
  • b/c of this requirement, these kinases are called cyclin-dependent kinases, or Cdks
17
Q

MPF

A
  • first cyclin-Cdk complex that was discovered (in frog eggs)
  • “maturation-promoting factor” but can be thought of as “M-phase-promoting factor” b/c it triggers the cell’s passage past G2 checkpt into M phase
  • when cyclins that accumulate during G2 associate w/ Cdk molecules, the resulting MPF complex phosphorylates a variety of proteins, initiating mitosis
  • MPF acts both directly as a kinase and indirectly by activating other kinases
18
Q

MPF activity

A

peaks during M, has fallen abruptly by G1, rises from S to M

19
Q

MPF termination

A
  • during anaphase, it switches itself off by initiating a process that leads to destruction of its own cyclin
  • the Cdk persists in the cell, inactive until it becomes part of MPF again by associating w/ new cyclin molecules synthesized during the S and G2 phases of the next round of the cycle
20
Q

MPF specific situations

A
  • MPF causes phosphorylation of various proteins of the nuclear lamina, which promotes fragmentation of the nuclear envelope during prometaphase of mitosis
  • MPF may contribute to molecular events required for chromosome condensation and spindle formation during prophase
21
Q

internal signal ex

A
  • occurs at M checkpt
  • anaphase doesn’t begin until all the chromosomes are properly attached to the spindle at the metaphase plate; as long as some kinetochores are unattached, the sister chromatids remain together, delaying anaphase
  • only when the kinetochores are properly attached to the spindle does the appropriate regulatory protein complex become activated
  • once activated, the complex sets off a chain of molecular events that activates SEPARASE, which cleaves the COHESINS, allowing the chromatids to separate
  • this mechanism ensures that daughter cells don’t end up w/ missing/extra chromosomes
22
Q

external signals

A
  • cells fail to divide is an essential nutrient is lacking in the culture medium
  • even if all other conditions are favorable, most types of mammalian cells divide in culture only if the growth medium includes specific growth factors
23
Q

PDGF

A
  • platelet-derived growth factor; made by blood cell fragments called platelets
  • PDGF required for division of FIBROBLASTS, a type of connective tissue cell
  • fibroblasts have PDGF receptors (RTKs) on their plasma membranes; binding of PDGF molecules to these receptors triggers a signal transduction pathway that allows the cells to pass G1 chekpt and divide
24
Q

PDGF stimulation

A

when an injury occurs, plateletts release PDGF in the vicinity. the resulting proliferation of fibroblasts helps heal the wound.

25
Q

density-dependent inhibition

A
  • phenomenon in which crowded cells stop dividing
  • cultured cells normally divide until they form a single layer of cells on the inner surface of the culture container; then they stop
  • if some cells are removed, those bordering the open space begin dividing again to fill the space
  • follow-up studies revealed that the binding of a cell-surface protein to its counterpart on an adjacent cell sends a growth-inhibiting signal to both cells, preventing them from moving forward in the cell cycle even in the presence of growth factors
26
Q

anchorage dependence

A
  • most animal cells exhibit this

- to divide, they must be attached to a sub-stratum

27
Q

“immortality” of cancer cells

A
  • can go on dividing indefinitely in culture if they’re given a continual supply of nutrients
  • HeLa cells (from a tumor taken from Henrietta Lacks) have been reproducing in culture since 1951
  • normal mammalian cells in culture divide only 20 - 50 times before stopping
28
Q

transformation

A
  • converts normal to cancer cell
  • immune system normally recognizes a transformed cell and destroys it; if cell evades destruction, it may proliferate and form a tumor, a mass of abnormal cells w/in otherwise normal tissue
29
Q

benign tumor

A

the abnormal cells may remain at the original site if they have too few genetic and cellular to survive at another site. don’t cause serious problems, can be completely removed w/ surgery

30
Q

malignant tumor

A

includes cells whose genetic and cellular changes enable them to spread to new tissues and impair the functions of one or more organs.

31
Q

cell surface changes

A

abnormal changes cause cancer cells to lose attachments to neighboring cells and the ECM, allowing them to spread into nearby tissues.

32
Q

metastasis

A
  • The spread of cancer cells to locations distant from their original site.
  • a few tumor cells may separate from original tumor, enter blood and lymph vessels, and travel to other parts of the body